Eosinophil infiltration, gastric juice and serum eosinophil cationic protein levels in Helicobacter pylori‐associated chronic gastritis and gastric ulcer

Abstract

INTRODUCTION: Helicobacter pylori is one of the main causes of gastroduodenal diseases, such as chronic gastritis and peptic ulcer. It has been shown that eosinophils increase in the stomach in H. pylori infection. Eosinophilic cationic protein (ECP) is a cytotoxic molecule secreted by the activated eosinophils. However, there are no sufficient data about the role of ECP in H. pylori infection and its effect on ulcer development. In this study we investigated the gastric eosinophilic infiltration, gastric juice and serum ECP levels in patients with chronic gastritis and gastric ulcer associated with H. pylori.Materials and methods: Forty‐four H. pylori‐positive and 20 H. pylori‐negative patients who underwent upper gastrointestinal system endoscopy after admitting with dyspeptic complaints were enrolled in the study. Twenty‐one of the H. Pylori‐positive patients had gastric ulcer while 23 patients had none. During endoscopy, multiple gastric biopsies and juices were taken. In gastric biopsies, H. pylori and eosinophilic infiltration were assessed. Additionally, gastric juice and serum ECP levels were measured.Results: Eosinophil infiltration, gastric juice ECP levels, and gastric juice/serum ECP ratios in the H. pylori‐positive group were greater than in the H. pylori‐negative group (p < 0.01). There was no statistically significant difference regarding serum ECP levels between the two groups (p > 0.05). When H. pylori‐positive patients were compared with regard to gastric ulcer presence, however, there was no significant difference in gastric eosinophil infiltration, gastric juice ECP levels, serum ECP levels, and gastric juice/serum ECP ratios (p > 0.05).Conclusion: The results of this study suggest that eosinophils and eosinophil‐released ECP may contribute to inflammatory changes seen in chronic gastritis, whereas there is no proof that they play a role in ulcer development.

Complete Blood Cell Parameters between Anti-HP IgG Antibody Positive and Negative Subjects

“…Although the percent of blood EOS count is higher in IgG positive group than IgG negative group, the correlation between anti-HP IgG antibody titers and EOS count is not significant in the present study. There are several studies that support our results in HP infection [21,22]. Activation of eosinophils seems to contribute to the pathophysiology of several inflammatory conditions [23].…”

“…The role of eosinophils in the pathogenesis of HP-associated gastritis and ulcer is not explained. One of the major constituents of the granule matrix is the eosinophil cationic protein [22]. Aydemir et al [22] reported that gastric mucosal eosinophil infiltration and the gastric juice ECP level were apparently greater in H. pylori infected subjects, however, serum ECP level no significant between H. pylori infected and non-infected groups.…”

“…One of the major constituents of the granule matrix is the eosinophil cationic protein [22]. Aydemir et al [22] reported that gastric mucosal eosinophil infiltration and the gastric juice ECP level were apparently greater in H. pylori infected subjects, however, serum ECP level no significant between H. pylori infected and non-infected groups. The presence of eosinophils is assumed as a protective mechanism of unspecific mucosal immunity response against bacteria and parasites [20,24].…”

A Player and Coordinator: The Versatile Roles of Eosinophils in the Immune System

“…Consistent findings were confirmed in a larger sample size by a later study with specimens from 44 H. pylori-positive patients and 20 H. pylori-negative patients [117]. In specimens of chronic H. pylori gastritis, the severity of gastritis was significantly correlated with that of eosinophil infiltration [116], although no difference in the severity of eosinophil infiltration was observed between gastritis with ulcer and those without gastric ulcer among H. pylori-positive patients [117].…”

Effect of the flavonoid quercetin on inflammation and lipid peroxidation induced by Helicobacter pylori in gastric mucosa of guinea pig

“…[1][2][3] The bacterial derivatives cause infl ammatory infi ltration in the stomach tissue consisting of neutrophil and eosinophil leukocytes, lymphocytes, plasma cells, and macrophages. [4][5][6] Several studies have indicated that H. pylori infection is accompanied by an infl ammatory response associated with gastric mucosal damage through the activation of polymorphonuclear neutrophil leukocytes. 7 In these cells the activation of enzymatic systems such as NADPH oxidase, inducible nitric oxide synthase, and myeloperoxidase form reactive species of oxygen and nitrogen, precursors of the production of hypochlorite, monochloramine, and peroxinitrite, with oxidative and cytolytic effects on the gastric mucosa.…”